Although several types of angiotensin II type 1 (AT1) receptor blockers (ARBs) are commercially available for the treatment of patients with hypertension, telmisartan could have the strongest binding affinity to AT1 receptor [1]. Furthermore, telmisartan acts as a selective peroxisome proliferator-activated receptor-γ (PPAR-γ) modulator when tested at concentrations that might be achievable with oral doses recommended for treatment of hypertension, whereas this property does not appear to be shared by other ARBs [2]. Telmisartan is a moderately potent selective PPAR-γ agonist, activating the receptor to 25–30% of the maximum level achieved by conventional full agonists, such as pioglitazone and rosiglitazone [3,4]. The identification of telmisartan as a unique AT1 receptor antagonist with selective PPAR-γ modulating ability suggests new opportunities for developing third generation ARBs and PPAR-γ activators, with enhanced potential for treating hypertension, diabetes, and metabolic syndrome [5]. A number of randomized trials of telmisartan versus other ARB therapy, however, have been inconclusive as to whether telmisartan improves insulin sensitivity. We performed the first metaanalysis of randomized head-to-head trials of telmisartan for reduction in fasting insulin level and improvement of insulin sensitivity. Public domain databases including MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials were searched through September 2011 using Web-based search engines (PubMed, OVID). Text keywords included telmisartan; azilsartan, candesartan, eprosartan, irbesartan, losartan, olmesartan, or valsartan; glucose, glycemic, euglycemia, euglycemic, insulin, minimal model, homeostasis, Matsuda, Stumvoll, Avignon, diabetes, diabetic, or metabolic syndrome; and; randomized, randomised, randomly, or randomization. Studies considered for inclusion met the following criteria: the design was a prospective randomized controlled clinical trial; the study population was unrestricted patients; patients were randomly assigned to telmisartan versus azilsartan, candesartan, eprosartan, irbesartan, losartan, olmesartan, or valsartan therapy; and main outcomes included fasting insulin level and/or data on insulin sensitivity as measured by euglycemic clamp, minimum model (MIDMOD), fasting sampled intravenous glucose tolerance test (FSIVGTT), insulin suppression test, quantitative insulin sensitivity check index (QUICKI), homeostasis model assessment (HOMA), Matsuda index, Stumvoll index, or Avignon index [6–10]. When more than one datum on insulin sensitivity was reported in a trial, HOMA of insulin resistance (HOMA-IR) was used preferentially as the study-specific measure because most trials reported it. For each study, data regarding the final value of insulin level and insulin sensitivity in both the telmisartan and other ARB groups were used to generate standardized mean differences (SMDs) and 95% confidence intervals (CIs). For the purposes of meta-analysis, the direction of data on insulin sensitivity for some studies (e.g. glucose infusion rate in euglycemic, hyperinsulinemic clamp) was reversed to ensure consistency of directionality between the tests, thus decreases in the SMD suggest improvements in insulin sensitivity in this meta-analysis whereas increases suggest worsening. Study-specific estimates were combined using inverse variance-weighted averages of logarithmic SMDs in both fixedand random-effects models. Between-study heterogeneity was analyzed by means of standard χ tests. Where significant statistical heterogeneity was identified, the random-effects estimate was used preferentially as the summary measure. Sensitivity analyses were performed to assess the contribution of each study to the pooled estimate by excluding individual trials one at a time and recalculating the pooled SMD estimates for the remaining studies. To assess the impact of differential length of follow-up on the studyspecific estimate, we developed a mixed-effects (unrestricted maximum likelihood) meta-regression model by plotting the SMD against the duration of follow-up. Publication bias was assessed graphically using a funnel plot and mathematically using an adjusted rankcorrelation and linear regression test. All analyses were conducted using Review Manager version 5.1 (Nordic Cochrane Centre, Copenhagen, Denmark) and Comprehensive Meta-Analysis version 2 (Biostat, Englewood, NJ). Our search identified 22 prospective randomized head-to-head clinical trials of telmisartan versus other ARB therapy [11–32]. The International Journal of Cardiology 156 (2012) 92–122